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PubMed1993

Hormonal factors in susceptibility to multiple sclerosis.

Evidence implies that hormonal factors are involved in susceptibility to multiple sclerosis. Diseases associated with a class II allele occur more frequently in women than in men. Multiple sclerosis is more frequent in women, particularly in the early- and late-onset groups. Pregnancy has a favorable effect on the course of multiple sclerosis on both a short- and a long-term basis. Experimental allergic encephalomyelitis, an animal model with similarities to multiple sclerosis, is also influenced by hormonal factors in both occurrence and severity. The multiple levels of interaction between immune, endocrine, neurologic, and genetic systems probably explain the action of sex steroids in multiple sclerosis susceptibility.

Alleles↗

PubMed1992

The association of cervical spondylosis and multiple sclerosis.

The diagnostic and therapeutic considerations produced by the coexistence of cervical spondylosis and multiple sclerosis are complex. We have encountered six patients, affected by both multiple sclerosis and cervical spondylosis, in whom neurosurgical procedures were performed. The diagnosis of multiple sclerosis was confirmed by a combination of clinical, neuroimmunologic, electrophysiologic, and neuroradiologic findings. The diagnosis of spondylosis with spinal cord compromise was confirmed by myelography and computed tomographic scan in all cases, and by magnetic resonance imaging in four. Surgery was followed by lasting clinical improvement in two patients, transient improvement in one, and no change in the other three. Our experience confirms that multiple sclerosis and cervical spondylosis can coexist and suggests that this coexistence may result in an interaction that compounds the deleterious effect on the nervous system. Diagnostic evaluations of patients, particularly young patients, with symptoms of cervical spondylosis should include consideration of the possible coexistence of multiple sclerosis. The evaluation of a patient with known multiple sclerosis who develops new signs of cervical spinal cord dysfunction should always include spinal neuroimaging studies. When progression of symptoms coincides with documented progression of anatomic compression, surgical intervention can yield good results.

Adult↗

PubMed1994

Usher's syndrome and multiple sclerosis. Review of an individual with Usher's syndrome with a multiple sclerosis-like illness.

We describe an individual with Type I Usher's syndrome and a multiple sclerosis-like illness. MRI scan showed vermian atrophy on T1-weighted images and multiple white matter lesions in the periventricular areas on T2-weighted images. Although MRIs demonstrating increased signal intensity on weighted images are reported in some individuals with Usher's syndrome, the cerebrospinal fluid findings are not described in these cases. In the present case, oligoclonal bands were present in the spinal fluid. The possibility of a linkage between the two diseases is raised.

Adult↗

PubMed1991

Immunopathologic features of retinal lesions in multiple sclerosis.

To further characterize the nature of retinal periphlebitis and retinitis in multiple sclerosis, immunoperoxidase studies were performed on retinal tissue from multiple sclerosis patients at autopsy. Antibodies against myelin basic protein stained the optic nerve but not the retina. Both normal and multiple sclerosis retinas showed staining of Müller cells with Leu-7 (a monoclonal antibody that cross-reacts with myelin associated glycoprotein and natural killer cells). Nerve fiber bundles of the optic nerve in cases with multiple sclerosis and controls also showed staining with Leu-7 antibody. Tissue-bound IgG was demonstrated on retinal ganglion cells in six of seven multiple sclerosis cases but not in controls.

Antibodies, Monoclonal↗

PubMedDate not supplied

[Prevalence of Helicobacter pylori infection among patients with multiple sclerosis].

A group of 90 subjects with multiple sclerosis was examined with the serological Helicotest for the presence of antibodies against Helicobacter pylori. Positive results were found in 17 patients (18.9%), which is markedly lower than this infection incidence rate in the population of Poland. The results indicate a lack of connection between the Helicobacter pylori infection and multiple sclerosis. However, it seems reasonable to perform the test in MS patients so as to avoid the risk of the upper alimentary tract complications in the course of intense steroid treatment applied as a standard management of multiple sclerosis relapse.

Adult↗

PubMed2006

The pathology of multiple sclerosis: a paradigm shift.

PURPOSE OF REVIEW: Detailed immunopathological assessment of multiple sclerosis tissue remains the research tool most likely to elucidate the major processes involved in disease pathogenesis and tissue injury. Such studies steer and provide the impetus for refining cellular/molecular investigations and developing more relevant disease models in animals. RECENT FINDINGS: Recent observations in early multiple sclerosis lesions challenge the traditional hypothesis that multiple sclerosis arises as the result of a primary autoimmune process that specifically targets myelin antigen(s). A new multiple sclerosis paradigm proposes that oligodendrocyte apoptosis is the earliest change in newly forming lesions and that tissue injury is amplified by the subsequent recruitment of a systemic immune response. Over months to years the pathology of multiple sclerosis is transformed and the changes which accompany the late phase of the disease suggest that the inflammatory response becomes progressively 'compartmentalized' and therefore largely isolated from systemic influence with time. SUMMARY: Recent pathological studies raise important questions regarding the aetiology of oligodendrocyte apoptosis, the mechanisms by which the accompanying inflammatory response amplifies tissue injury and the regulation of central nervous system immunity. An improved understanding of these processes is essential for advancing therapeutic interventions applicable to different stages of the disease.

Animals↗

PubMed1997

An electrophysiological study of the mechanism of fatigue in multiple sclerosis.

Fatigue is a common and disabling symptom in multiple sclerosis but is poorly understood. We investigated 'physiological' fatigue in 21 patients with multiple sclerosis who complained of disabling fatigue by measuring the decline in strength during a 45 s maximal contraction of the adductor pollicis muscle. The results were compared with those from a control group of 19 healthy subjects. The strength of control subjects declined by approximately 20% during the contraction; twitch interpolation showed central drive remained almost maximal throughout, and therefore that the fatigue was peripheral in origin. Patients had normal baseline strength, but developed greater fatigue (approximately 45%), which was central in origin. In both cases, the decline in strength followed a roughly linear time course suggesting that the patients, like the normals, were trying to maintain a maximum voluntary effort. Evidence for frequency-dependent conduction block (FDCB) in the patients' central motor pathways was sought by measuring the EMG responses to single and paired transcranial magnetic stimuli. Fatigue had no effect on the latency or size of EMG responses to transcranial magnetic stimulation, suggesting that FDCB was unlikely to have occurred. This was supported by measurements of the maximum speed of voluntary muscle contraction; although the patients showed relatively slow speeds before exercise, the decline in speed after fatigue was no greater than in normal subjects. We conclude that excessive 'physiological' fatigue contributes to the symptom of fatigue in multiple sclerosis and is central in origin. However, since the degree of exercise-induced fatigue did not correlate with the baseline complaint of fatigue, other factors must also be operating to produce the full range of clinical symptoms. We found no conclusive evidence that central fatigue is related to increased dysfunction in the primary central motor pathways and no evidence that FDCB is the pathophysiological mechanism. We postulate that central fatigue in multiple sclerosis is due to impaired drive to the primary motor cortex and several lines of evidence strongly suggest that this is not due to a lack of motivation.

Adult↗

PubMed1992

Economic status of families living with multiple sclerosis.

A nation-wide survey of 604 families living with multiple sclerosis was conducted. The sample was recruited through local chapters of the National Multiple Sclerosis Society and the public press. This paper describes the economic impact of the disease on families. There were 427 families in which the woman had multiple sclerosis and 177 families in which the man had the disease. The average duration of the disease was 10 years. Family income was well above the national median income. Thirty-nine per cent of the men and 19% of the women with multiple sclerosis retired because of disability. Income was inadequate to pay for medical expenses in 21% of the families and 25% had inadequate funds to meet basic living expenses. While 80% of the families had health care insurance, for 28% of the families the insurance was inadequate to cover the cost of their illness. The number of children living at home and the amount of health care bills paid out-of-pocket failed to explain why families in the high income group had difficulty meeting their expenses. Factors other than income and proportion of medical expenses covered by insurance determine the economic impact on the family. If health care providers are going to meet all the needs of a family living with multiple sclerosis, a more comprehensive assessment of their economic status is needed.

Adult↗

PubMed1996

Augmented expression of tumour necrosis factor-alpha and lymphotoxin in mononuclear cells in multiple sclerosis and optic neuritis.

The involvement of proinflammatory cytokines tumour necrosis factor-alpha (TNF-alpha) and lymphotoxin (LT) in multiple sclerosis is suggested by the parallel occurrence of these proinflammatory cytokines in acute and chronic active multiple sclerosis brain lesions. We describe the use of in situ hybridization with radiolabelled cDNA oligonucleotide probes to detect and enumerate TNF-alpha and LT mRNA expressing mononuclear cells without culture, and after culture in the presence of myelin basic protein (MBP), control antigens or without antigen. Compared with patients with aseptic meningo-encephalitis, non-inflammatory neurological diseases and healthy controls, the multiple sclerosis patients had elevated numbers of TNF-alpha and LT mRNA expressing mononuclear cells in blood when enumerated without previous culture, and also after culture with MBP. The MBP-induced upregulation of TNF-alpha and LT was major histocompatibility complex (MHC) class II molecule dependent. Tumour necrosis factor-alpha mRNA expressing mononuclear cells were further enriched in the multiple sclerosis patients' CSF. Positive correlations were observed in multiple sclerosis between TNF-alpha and LT mRNA expressing blood mononuclear cells, MBP-reactive TNF-alpha and LT mRNA expressing cells, and TNF-alpha and interferon-gamma (INF-gamma) mRNA expressing mononuclear cells. Upregulation of TNF-alpha correlated positively with exacerbation, enhanced disability and the secondary progressive phase of multiple sclerosis. Patients with optic neuritis, in many instances representing very early multiple sclerosis, had TNF-alpha and LT positive blood mononuclear cells that were elevated to the same extent as patients with clinically definite multiple sclerosis. The findings support the hypothesis that TNF-alpha and LT play a harmful role in the development of multiple sclerosis and suggest that TNF-alpha could be useful as a disease activity marker in multiple sclerosis.

Adult↗

PubMed1995

The treatment of multiple sclerosis: current and future.

During the past year observations have been published that might lead to further improvement in the design of future clinical trials. At the same time, results of clinical trials have become available that suggest that a number of treatments could be of benefit in the care of patients in the various phases of multiple sclerosis. Future multiple sclerosis clinical trials should involve a blinded investigator restricted to assessing the clinical outcome variables, and because current evidence suggests that magnetic resonance imaging gives an objective and sensitive reflection of the biological evolution of the disease, such scanning should also be included. The use of a composite outcome variable in a trial of chronic progressive multiple sclerosis should also be considered in order to increase the percentage of patients reaching the clinical endpoint. In 1994 recommendations were published for the selection of relapsing-remitting patients for treatment with interferon beta-1b; furthermore, large and well performed clinical trials demonstrated that interferon beta-1a and copolymer-1 are also partially effective, though not curative, for these patients. Two smaller studies suggested that low-dose methotrexate and cladribine might have a beneficial effect on the course of the disease in patients with secondary chronic progressive multiple sclerosis, the former drug probably being less toxic. Unfortunately, therapeutic perspectives for patients with primary progressive multiple sclerosis are less promising at present. Several studies suggest that 4-aminopyridine and tizanidine have therapeutic potential for symptomatic treatment; the former by improving neurological deficits, the latter by relieving troublesome spasticity.(ABSTRACT TRUNCATED AT 250 WORDS)

Adjuvants, Immunologic↗

PubMed2005

Unrecognised symptoms of depression in a community-based population with multiple sclerosis.

BACKGROUND AND AIMS: The association between multiple sclerosis (MS) and depression has been well established but prevalence estimates have varied widely. The aims of this study were to assess the point prevalence of previously unrecognised symptoms of depression in a community-based population with MS and examine their relationship to other disease characteristics. PATIENTS AND METHODS: Three hundred and seventy six patients with clinically definite or probable MS (Poser criteria) were ascertained during the course of an epidemiological study on two counties in Ireland. Of these 211 agreed to participate in the study. Subjects were examined and a Kurtzke Expanded Disability Status Scale Score and Multiple Sclerosis Functional Composite score rated. Participants also completed a Beck's Depression Inventory-II and a Multiple Sclerosis Impact Scale. RESULTS: In total 60 (28%) patients had moderate or severe symptoms of depression. Only thirty-five of the 211 patients had a history of depression as defined by a medical diagnosis of depression or prescription of an anti-depressant medication at any time prior to enrollment in the present study, of the remaining 176 patients, 41 (23.3%) had moderate or severe symptoms of depression as assessed by Beck's Depression Inventory-II. The only significant clinical difference between the 41 patients with pronounced depressive symptoms and the 135 less affected was shorter disease duration in the former. CONCLUSIONS: In this study one in four patients with MS had unrecognised and therefore untreated symptoms of depression. Disability alone is not a good indicator of the likelihood of coexistent depressive symptoms.

Adult↗

PubMed2002

Patients with multiple sclerosis and risk of type 1 diabetes mellitus in Sardinia, Italy: a cohort study.

BACKGROUND: Individuals from Sardinia, Italy, are at high risk of developing multiple sclerosis and type 1 diabetes mellitus. We attempted to assess the prevalence in this region of type 1 diabetes mellitus in individuals with multiple sclerosis, and to ascertain disease risk factors. METHODS: We did a cohort study to assess prevalence of type 1 diabetes in 1090 people with multiple sclerosis, and in their parents (n=2180) and siblings (n=3300), all born and living in Sardinia. All participants were patients at the multiple sclerosis clinic in Cagliari, and were judged representative of the total Sardinian outpatients and inpatients. We asked patients whether their parents or siblings had multiple sclerosis or diabetes, confirming replies by examining clinical records. We identified risk factors for diabetes with univariate and multivariate logistic regression analyses. FINDINGS: Diabetes prevalence in people with multiple sclerosis was, respectively, about three-fold and five-fold that in their healthy siblings (p=0.001) and in the general population (p<0.0001). Presence of other relatives with multiple sclerosis conferred increased risk of type 1 diabetes to healthy siblings of individuals with multiple sclerosis (odds ratio=3.41, p=0.0019). Diabetes risk was six-fold higher in patients with relatives having multiple sclerosis than in healthy siblings of multiple sclerosis patients without other relatives with the disease (p=0.0001). INTERPRETATION: In Sardinian families with genetic inheritance of multiple sclerosis type 1 diabetes is prevalent, both in multiple sclerosis patients and in healthy siblings. This finding indicates that common genes contribute to susceptibility to both diseases in this population.

Adolescent↗

PubMed1999

[Mortality due to multiple sclerosis in Spain, 1951-1992].

UNLABELLED: FOUNDATIONS: In this work, multiple sclerosis mortality trend in Spain from 1951 to 1992 is displayed. The purpose is to identify the pattern of age-adjusted mortality evolution and to measure the effect of environmental factors. METHODS: Multiple sclerosis mortality is standardized by age using the world standard population. In each year from 1951 to 1992, age-specific mortality rates are transversely fitted to the Gompertz law. The Longitudinal Gompertzian analysis is applied to the obtained coefficients to quantify the effects of competing risks and environmental factors. RESULTS: Multiple sclerosis age-adjusted mortality increased from 1951 to 1968; a step-down is produced in 1969 (coinciding with change from 7th to 8th revision of the International Classification of Diseases) and a stability from 1970 on. Multiple sclerosis in Spain is a Gompertzian disease. Adjusting mortality for R0 (which in the Gompertz function represents the addition of the environmental factors acting in a point near the beginning of the life and the competing risks of death) the result was almost constant throughout the whole analyzed period. CONCLUSIONS: It is suggested that multiple sclerosis mortality trend in Spain is due to changes in some environmental factor acting early and in a point; on the other hand, diet or other environmental factors acting for long time or genetic factors have and little or no influence in this trend.

Adult↗

PubMed2005

Evidence of elevated glutamate in multiple sclerosis using magnetic resonance spectroscopy at 3 T.

Histopathological reports of multiple sclerosis and its animal models have shown evidence of a link between axonal injury in active lesions and impaired glutamate metabolism. Mature oligodendrocytes play a role in glutamate uptake to maintain glutamate homeostasis but in multiple sclerosis white matter the loss of expression of glutamate transporters in the lesion vicinity results in ineffective glutamate removal. Using a magnetic resonance spectroscopy technique that isolates the glutamate resonance at 3 T, we compared glutamate levels between normal subjects and multiple sclerosis patients in different brain areas. Metabolite concentrations (glutamate, glutamine, N-acetyl-aspartate, myo-inositol, choline, creatine) were derived from LCmodel and corrected for T1 relaxation time. Glutamate concentrations were found to be elevated in acute lesions (P = 0.02) and normal-appearing white matter (P = 0.03), with no significant elevation in chronic lesions (P = 0.77). The N-acetyl-aspartate level in chronic lesions was significantly lower (P < 0.001) than in acute lesions and normal-appearing white matter. The choline level in acute lesions was significantly higher (P < 0.001) than in chronic lesions. Evidence was also found for increased glial activity in multiple sclerosis, with significantly higher (P < 0.001) myo-inositol levels in acute lesions compared with control white matter. These in vivo results support the hypothesis that altered glutamate metabolism is present in brains of multiple sclerosis patients.

Acute Disease↗

PubMed1996

Treatment of refractory urge urinary incontinence with sacral spinal nerve stimulation in multiple sclerosis patients.

BACKGROUND: Urge urinary incontinence in multiple sclerosis patients is usually due to detrusor hyperreflexia. Patients who do not respond to conservative measures such as anticholinergics, with or without clean intermittent catheterisation, are difficult to manage. METHODS: We applied electrical stimulation to the S3 sacral spinal nerves with the aim of activating afferent somatic nerve fibres. Stimulation of these fibres can inhibit the micturition reflex. An S3 electrode coupled to a subcutaneously placed pulse generator was implanted in four women who had shown a good response during temporary stimulation via a percutaneously placed wire electrode. All patients were followed for at least 2 years. FINDINGS: The number of leakage episodes decreased from a mean of 4 to 0.3 per 24 h. Two patients were completely dry. The hyperreflexia disappeared in one, improved in two, and got worse in one patient. The urodynamic result in the last patient may be explained by clinical progression of the multiple sclerosis. INTERPRETATION: Chronic stimulation of the S3 sacral spinal nerve by an implantable neuroprosthesis is a promising treatment option for selected multiple sclerosis patients with refractory urge incontinence.

Adult↗

PubMed1989

The prevalence of primary Sjögren's syndrome in a multiple sclerosis population.

A central nervous system illness closely resembling multiple sclerosis has been described in patients with primary Sjögren's syndrome. From these reports, the estimated prevalence of this syndrome could be similar to that of multiple sclerosis in a high-frequency area. We evaluated 192 consecutive patients in our multiple sclerosis clinic to determine if such cases had gone unrecognized. We did not find any patients with clinical or serological evidence of primary Sjögren's syndrome. We conclude that it is rare for neurological manifestations of Sjögren's syndrome to mimic multiple sclerosis in our population.

Adult↗

PubMed1975

[Bladder and rectum disturbances in multiple sclerosis].

Bladder and bowel dysfunction in multiple sclerosis. In a group of 88 unselected patients suffering from multiple sclerosis the incidence and type of neurogenic bladder and bowel dysfunctions, the reliability of subjective complaints and the relationship between these disorders and neurological signs were investigated. The bladder function was proved by a cystometry, in some cases also by an uroflowmetry. Cases with bladder neck obstructions caused by tumours were eliminated. The results demonstrate the incidence of 58% subjective bladder disorders. Urinary retention was found in 60%, pathological results in cystometry only in 46% in contrast to literature findings with a higher amount of pathological results in cystometry. It should be emphasized the dissociation between subjective complaints and proved bladder disorders in 25% of the patients. Bladder and bowel disorders appear more frequent if the neurological syndrome is characterized by perception disorders.

Defecation↗

PubMed2007

Multiple sclerosis after infectious mononucleosis.

BACKGROUND: Infectious mononucleosis caused by the Epstein-Barr virus has been associated with increased risk of multiple sclerosis. However, little is known about the characteristics of this association. OBJECTIVE: To assess the significance of sex, age at and time since infectious mononucleosis, and attained age to the risk of developing multiple sclerosis after infectious mononucleosis. DESIGN: Cohort study using persons tested serologically for infectious mononucleosis at Statens Serum Institut, the Danish Civil Registration System, the Danish National Hospital Discharge Register, and the Danish Multiple Sclerosis Registry. SETTING: Statens Serum Institut. PATIENTS: A cohort of 25 234 Danish patients with mononucleosis was followed up for the occurrence of multiple sclerosis beginning on April 1, 1968, or January 1 of the year after the diagnosis of mononucleosis or after a negative Paul-Bunnell test result, respectively, whichever came later and ending on the date of multiple sclerosis diagnosis, death, emigration, or December 31, 1996, whichever came first. MAIN OUTCOME MEASURE: The ratio of observed to expected multiple sclerosis cases in the cohort (standardized incidence ratio). RESULTS: A total of 104 cases of multiple sclerosis were observed during 556,703 person-years of follow-up, corresponding to a standardized incidence ratio of 2.27 (95% confidence interval, 1.87-2.75). The risk of multiple sclerosis was persistently increased for more than 30 years after infectious mononucleosis and uniformly distributed across all investigated strata of sex and age. The relative risk of multiple sclerosis did not vary by presumed severity of infectious mononucleosis. CONCLUSIONS: The risk of multiple sclerosis is increased in persons with prior infectious mononucleosis, regardless of sex, age, and time since infectious mononucleosis or severity of infection. The risk of multiple sclerosis may be increased soon after infectious mononucleosis and persists for at least 30 years after the infection.

Adult↗